Soluble Jagged-1 inhibits restenosis of vein graft by attenuating Notch signaling
| Autor: | Yong-guang Xiao, Jie Huang, Qing Geng, Wei Wang, Ping Dong, Zhifu Mao, Xinming Zhou |
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| Rok vydání: | 2014 |
| Předmět: |
Male
medicine.medical_specialty Vascular smooth muscle Intimal hyperplasia Time Factors Carotid Artery Common Myocytes Smooth Muscle Notch signaling pathway Apoptosis Transfection Biochemistry Muscle Smooth Vascular Restenosis In vivo Jugular vein medicine.artery Neointima Medicine Animals Serrate-Jagged Proteins Common carotid artery Rats Wistar Receptor Notch1 Cells Cultured Cell Proliferation business.industry Calcium-Binding Proteins Graft Occlusion Vascular Membrane Proteins Cell Differentiation Cell Biology Genetic Therapy medicine.disease Surgery Disease Models Animal Phenotype cardiovascular system Cancer research Intercellular Signaling Peptides and Proteins Vascular Grafting Jugular Veins Cardiology and Cardiovascular Medicine business Jagged-1 Protein Signal Transduction |
| Zdroj: | Microvascular research. 100 |
| ISSN: | 1095-9319 |
| Popis: | The excessive proliferation of vascular smooth muscle cells was key factor in the restenosis of vein graft. And the Notch signaling was demonstrated to regulate vSMC proliferation and differentiation. Soluble Jagged-1 (sJag1) can inhibit Notch signaling in vitro and in vivo; however, its capacity to suppress restenosis of vein graft remains unknown. Under the microscope, the left jugular vein of these rats was interposed into the left common carotid artery, followed without any treatment (control), or with Ad-Jag1 (treatment) or placebo (DMSO) post operation. We showed that Ad-Jag1 can attenuate restenosis of vein graft by inducing decreased proliferation and increased apoptosis in vivo. Notch1-Hey2 signaling is critical for the development of intima thickening by controlling vSMC-fate determination. By blocking Notch signaling, Ad-Jag1 can significantly inhibit intima thickening. These studies identify that Ad-Jag1 can restore the vSMC phenotype and inhibit the vSMC proliferation by suppression of Notch1 signaling, and thus open a new avenue for the treatment of restenosis in vein graft. |
| Databáze: | OpenAIRE |
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